Amanita caesarea, Caerer's mushroom, Tom Volk's Fungus of the Month for March 2002 Tom Volk's Fungus of the Month for March 2002 This month's fungus is Amanita caesarea, Caesar's mushroom. For the rest of my pages on fungi, please click TomVolkFungi.net Beware the Ides of March. Amanita is a well-defined genus of mycorrhizal Agaricales (gill forming mushrooms) that have a white spore print, gills (lamellae) that are free from the stipe (stalk) and a universal veil covering the young mushroom buttons. When the mushroom expands, the universal veil is broken; the bottom of the universal veil forms the cup shaped volva at the base of the mature mushroom. The top of the universal veil is often left at the top of the mushroom cap, forming a patch or sometimes breaking up into scaly floccules. Most species also have a partial veil, a membranous structure that protects the developing gills of the young mushroom. When the mushroom cap expands, the partial veil breaks and is left as a ring (annulus) on the stalk.

See the picture to the right for labeling of these various parts of the mature mushrooms and the expanding button. Some Amanita species, such as A. fulva and A. vaginata lack the partial veil and annulus. Almost all other genera of mushrooms lack the universal veil and volva-- a notable exception is Volvariella, but that genus has a pink spore print and always grows on wood or other debris, including other mushrooms. As you might guess from the name, Amanita caesarea was a favorite of the emperors of the Roman Empire, the Caesars. Perhaps Julius Caesar ate a meal of this delicious mushroom before Brutus did him in on the Ides of March (March 15). Et tu Brute? However, the most famous killing involving Amanita took place in ancient Rome circa 50-60 A.D. The Emperor Claudius had ascended to the throne after the assassination of his nephew Caligula. We've all heard about the decadence (and Roman porno movies, such as "Veni, Vidi, Veni") associated with Caligula.

Anyway, Claudius had several wives, but finally married his fourth wife Agrippina, who was also his niece. Agrippina already had a son from a previous marriage, Nero, for whom she had great plans. She persuaded Claudius to adopt Nero, putting him in line for the throne, should something happen to Claudius. (You can see where this is going already.) Agrippina was an impatient woman, and could not wait for a natural death for Claudius; she plotted to kill him by feeding Claudius his favorite meal, Amanita caesarea, laced with extracts from Amanita phalloides, the death cap. When the symptoms set in the next day, a co-conspirator doctor Xenophon administered an enema of colocynth, a potent toxin from a plant called bitter apple, which together with the mushroom toxin killed Claudius. Nero and his fiddle thus became emperor, and the rest, as they say, is history. It is pretty well accepted that true Amanita caesarea does not exist in North America, having been described from the Italian region.

So although Amanita caesarea is the fungus of the month, none of the picture on this page are really Amanita caesarea. To the right is (probably) Amanita hemibapha from Texas; the pictures above, from Connecticut, are likely Amanita jacksonii. These two species are collective called the "American Caesar's Mushroom." As currently circumscribed, Amanita species are very narrowly defined, and species identification is difficult, at best. There are significant microscopic differences between the three species, and until someone does the molecular (DNA) studies on this group, we should consider them to be different species. The picture to the right also illustrates why you should carefully dig under mushrooms when you are collecting them. If you just pulled these mushrooms out by their stems you might miss the diagnostic character, the volva. Looking back at the pictures on this page, I should also point out that these mushrooms are *much* more beautiful when you see live fresh specimens. There are also much better, very beautiful pictures of these mushrooms in existence, but I do not see this mushroom very often-- never in Wisconsin. I hope you enjoyed learning something about Amanita caesarea and its relatives today.

There's lots of history behind some of our most beautiful mushrooms. Thanks to Dr. Debby Hanmer, plant pathologist in my department, for giving me the idea to have Caesar's mushroom commemorating the Ides of March. Anyone else have an idea for a future FOTM? If you have anything to add, or if you have corrections or comments, please write to me at volk.thom@uwlax.edu This page and other pages are © Copyright 2002 by Thomas J. Volk, University of Wisconsin-La Crosse. Return to Tom Volk's Fungi Home Page -- TomVolkFungi.net Death cap mushrooms: What do they look like and where are they found? - ABC News (Australian Broadcasting Corporation) Death cap mushrooms: What do they look like and where are they found? Updated February 27, 2015 17:36:41 Map: ACT The death cap mushroom, Amanita phalloides, is a deadly fungus commonly mistaken for edible mushrooms. The poisonous fungus is usually found during autumn but wet weather has prompted its early arrival in 2015. So what do we know about this little fungus? How dangerous is the death cap?

Ingesting one death cap mushroom is enough to kill a healthy adult. All parts of the mushroom are poisonous; cooking or peeling does not make the mushroom safe to eat. There is no way to remove the poison from the mushroom. The poisonous compounds are extremely stable. You cannot remove them by soaking, cooking or drying. The poisons are found throughout the cap, gills, stem and spores. What does it look like? Photo: The caps are not yet fully expanded on these young specimens. (ABC News: Penny McLintock ) The caps of the mushrooms are 40-160mm wide, usually pale green to yellow in colour, with distinctive white gills and white stem. It has a membranous skirt on the upper part of the stem and a cup-like structure around the base of the stem (called a volva). Sometimes the bulbous base and the volva are partially buried in the soil or hidden by grass and leaf litter. The cap may be slippery and sticky to touch and shiny when dry. Variations can see the cap an olive to light brown colour. "It also always has a slight ammonia-like smell, sometimes quite pronounced like household ammonia," said fungi expert Heino Lepp.

Mr Lepp, who is an honorary scientific associate at the Australian National Botanic Gardens, said the death cap was easily identifiable to those experienced in identifying mushrooms. But he said it was better to err on the side of caution and avoid picking wild mushrooms during autumn. He said there were far more "unknowns than knowns" when it comes to native Australian mushrooms. "In Canberra because we have a mix of native vegetation as well as exotic vegetation, a lot of mushrooms grow in association with trees," he said. "There are a lot of unknown species of Australian mushrooms. Australia has quite a number of native amanita species which grow in symbiotic association with gum trees of which nothing is known about the toxicity. "It would be surprising if there weren't native species that were poisonous." Where is it found? Death caps are common in many Canberra suburbs and can be found growing near established oak trees during warm, wet autumn weather. It is also well-established in several Melbourne suburbs and in some Victorian country towns near Melbourne. It is not native to Australia and was accidentally introduced from the northern hemisphere. Death cap v straw mushroom The straw mushroom (Volvariella volvacea) is grown and eaten throughout Asia but it does not grow naturally in Australia.

However the species Volvariella speciosa is found naturally in many parts of Australia and looks very similar to the straw mushroom. Each species of Volvariella has a volva at the base of the stem and the gills do not reach the stem - just like the death cap. But with Volvariella there is no ring on the stem and the gills are pale pinkish-brown, rather than white. The cap is also more brown to greyish and more-or-less conical. However you could easily overlook some of these differences in a hasty examination and much depends on the weather. Mr Lepp said some Asian migrants or new Canberra residents pick death caps accidentally. "If you've grown up with straw mushrooms and think you recognise them, you might go and pick one of these and think you know what it is," he said. Photo: A half open death cap mushroom (Amanita phalloides) (left) beside a Volvariella speciosa (right) growing in Canberra. (Heino Lepp) What are the symptoms of death cap poisoning? Symptoms of poisoning generally appear between six and 24 hours after ingesting the death cap and can begin with nausea, vomiting and diarrhoea.

Those who fall ill can improve after a day or two, giving a false impression of recovery. But by that stage the toxin can have caused serious liver damage which can be fatal. Death cap poisoning is considered a medical emergency. If you suspect you have eaten some go to hospital immediately. If possible, take a sample of the mushroom with you. If you need more information or assistance regarding a suspected poisoning call the Poisons Information Centre on 13 11 26 (24 hours a day, seven days a week). The Death Cap - Amanita phalloides - Details - Encyclopedia of Life Learn more about this article This is one of the most poisonous European toadstools (3). All parts of the fungus are deadly, and it should never be eaten (4). The cap is typically yellowish to olivaceous green, sometimes paling almost to white, usually with darker streaks radiating outwards (3) (4) (5). It is convex at first, but becomes flattened as it ages, and may develop a sickly sweet smell (2) (5). The gills underneath the cap are white, and the white stem has a distinct ring, although this may become damaged or lost (3) (4).

The base of the stem bulges into a 'bulb', which is covered by a white sheath known as a volva (2). WARNING: Many species of fungus are poisonous or contain chemicals that can cause sickness. Never pick and eat any species of fungus that you cannot positively recognise or are unsure about. Some species are deadly poisonous and can cause death within a few hours if swallowed. © Wildscreen Learn more about this article A mycorrhiza (Greek for fungus roots; typically seen in the plural forms mycorrhizae or mycorrhizas) is a symbiotic (occasionally weakly pathogenic) association between a fungus and the roots of a plant (Kirk et al. 2001). In a mycorrhizal association the fungus may colonize the roots of a host plant either intracellularly or extracellularly. This mutualistic association provides the fungus with relatively constant and direct access to mono- or dimeric carbohydrates, such as glucose and sucrose produced by the plant in photosynthesis (Harrison 2005). The carbohydrates are translocated from their source location (usually leaves) to the root tissues and then to the fungal partners.

In return, the plant gains the use of the mycelium's very large surface area to absorb water and mineral nutrients from the soil, thus improving the mineral absorption capabilities of the plant roots (Selosse et al. 2006). Plant roots alone may be incapable of taking up phosphate ions that are immobilized, for example, in soils with an basic pH. The mycelium of the mycorrhizal fungus can however access these phosphorus sources, and make them available to the plants they colonize (Li et al. 2006). The mechanisms of increased absorption are both physical and chemical. Mycorrhizal mycelia are much smaller in diameter than the smallest root, and can explore a greater volume of soil, providing a larger surface area for absorption. Also, the cell membrane chemistry of fungi is different from that of plants. Mycorrhizae are especially beneficial for the plant partner in nutrient-poor soils. Mycorrhizal plants are often more resistant to diseases, such as those caused by microbial soil-borne pathogens, and are also more resistant to the effects of drought. These effects are perhaps due to the improved water and mineral uptake in mycorrhizal plants.

Mycorrhizae form a mutualistic relationship with the roots of most plant species (although only a small proportion of all species have been examined, 95% of all plant families are predominantly mycorrhizal) (Trappe 1987). Plants grown in sterile soils and growth media often perform poorly without the addition of spores or hyphae of mycorrhizal fungi to colonise the plant roots and aid in the uptake of soil mineral nutrients. The absence of mycorrhizal fungi can also slow plant growth in early succession or on degraded landscapes (Jeffries et al. 2003). References Harrison MJ (2005). Signaling in the arbuscular mycorrhizal symbiosis. Annu Rev Microbiol. 59: 19-42. Jeffries, P; Gianinazzi, S; Perotto, S; Turnau, K; Barea, J-M (2003). "The contribution of arbuscular mycorrhizal fungi in sustainable maintenance of plant health and soil fertility". Biol. Fertility Soils 37: 1-16. Kirk, P.M., P.F.

Cannon, J.C. David & J. Stalpers 2001. Ainsworth and Bisby’s Dictionary of the Fungi. 9th ed. CAB International, Wallingford, UK. Li H, Smith SE, Holloway RE, Zhu Y, Smith FA. (2006). Arbuscular mycorrhizal fungi contribute to phosphorus uptake by wheat grown in a phosphorus-fixing soil even in the absence of positive growth responses. New Phytol. 172: 536-543. Selosse MA, Richard F, He X, Simard SW (2006). Mycorrhizal networks: des liaisons dangereuses?. Trends Ecol Evol. 21: 621-628. Trappe, J. M. 1987. Phylogenetic and ecologic aspects of mycotrophy in the angiosperms from an evolutionary standpoint. Ecophysiology of VA Mycorrhizal Plants, G.R.

Safir (EDS), CRC Press, Florida Wikipedia Learn more about this article Fungi are not able to ingest their food like animals do, nor can they manufacture their own food the way plants do. Instead, fungi feed by absorption of nutrients from the environment around them. They accomplish this by growing through and within the substrate on which they are feeding. Numerous hyphae network through the wood, cheese, soil, or flesh from which they are growing. The hyphae secrete digestive enzymes which break down the substrate, making it easier for the fungus to absorb the nutrients which the substrate contains. This filamentous growth means that the fungus is in intimate contact with its surroundings; it has a very large surface area compared to its volume. While this makes diffusion of nutrients into the hyphae easier, it also makes the fungus susceptible to dessication and ion imbalance. But usually this is not a problem, since the fungus is growing within a moist substrate. Most fungi are saprophytes, feeding on dead or decaying material. This helps to remove leaf litter and other debris that would otherwise accumulate on the ground. Nutrients absorbed by the fungus then become available for other organisms which may eat fungi.

A very few fungi actively capture prey, such as Arthrobotrys which snares nematodes on which it feeds. Many fungi are parastitic, feeding on living organisms without killing them. Ergot, corn smut, Dutch elm disease, and ringworm are all diseases caused by parasitic fungi. University of California Museum of Paleontology Trusted Learn more about this article The species is now known to contain two main groups of toxins, both multicyclic (ring-shaped) peptides, spread throughout the mushroom tissue: the amatoxins and the phallotoxins. Another toxin is phallolysin, which has shown some hemolytic (red blood cell–destroying) activity in vitro. An unrelated compound, antamanide, has also been isolated. Amatoxins consist of at least eight compounds with a similar structure, that of eight amino-acid rings; they were isolated in 1941 by Heinrich O. Wieland and Rudolf Hallermayer of the University of Munich (Litten 1975).

Of the amatoxins, α-amanitin is the chief component and along with β-amanitin is likely responsible for the toxic effects (Köppel 1993; Dart 2004). Their major toxic mechanism is the inhibition of RNA polymerase II, a vital enzyme in the synthesis of messenger RNA (mRNA), microRNA, and small nuclear RNA (snRNA). Without mRNA essential protein synthesis and hence cell metabolism grind to a halt and the cell dies (Karlson-Stiber & Persson 2003). The liver is the principal organ affected, as it is the organ which is first encountered after absorption in the gastrointestinal tract, though other organs, especially the kidneys, are susceptible (Benjamin 1995). The RNA polymerase of Amanita phalloides is insensitive to the effects of amatoxins; as such, the mushroom does not poison itself (Horgen et al. 1978). The phallotoxins consist of at least seven compounds, all of which have seven similar peptide rings.

Phalloidin was isolated in 1937 by Feodor Lynen, Heinrich Wieland's student and son-in-law, and Ulrich Wieland of the University of Munich. Though phallotoxins are highly toxic to liver cells (Wieland & Govindan 1974), they have since been found to have little input into the death cap's toxicity as they are not absorbed through the gut (Karlson-Stiber & Persson 2003). Furthermore, phalloidin is also found in the edible (and sought-after) Blusher (Amanita rubescens) (Litten 1975). Another group of minor active peptides are the virotoxins, which consist of six similar monocyclic heptapeptides (Vetter 1998). Like the phallotoxins they do not exert any acute toxicity after ingestion in humans(Karlson-Stiber & Persson 2003). References Benjamin, Denis R. (1995). Mushrooms: poisons and panaceas — a handbook for naturalists, mycologists and physicians. New York: WH Freeman and Company.

Dart, RC (2004). "Mushrooms", Medical toxicology. Philadelphia: Williams & Wilkins, 1719–35. Horgen, Paul A.; Allan C. Vaisius and Joseph F. Ammirati (1978). "The insensitivity of mushroom nuclear RNA polymerase activity to inhibition by amatoxins". Archives of Microbiology 118 (3): 317–9. Karlson-Stiber C, Persson H (2003). "Cytotoxic fungi - an overview". Toxicon 42 (4): 339-49. Köppel C (1993). "Clinical symptomatology and management of mushroom poisoning". Toxicon 31 (12): 1513–40. Litten, W. (March 1975). "The most poisonous mushrooms". Scientific American 232 (3): 90–101. Vetter, János (January 1998). "Toxins of Amanita phalloides". Toxicon 36 (1): 13–24.

Wieland T, Govindan VM (1974). "Phallotoxins bind to actins". FEBS Lett. 46 (1): 351-3. Wikipedia Learn more about this article Mushroom poisoning is caused by the consumption of raw or cooked fruiting bodies (mushrooms, toadstools) of a number of species of higher fungi. The term toadstool (from the German Todesstuhl, death's stool) is commonly given to poisonous mushrooms, but for individuals who are not experts in mushroom identification there are generally no easily recognizable differences between poisonous and nonpoisonous species. Old wives' tales notwithstanding, there is no general rule of thumb for distinguishing edible mushrooms and poisonous toadstools. The toxins involved in mushroom poisoning are produced naturally by the fungi themselves, and each individual specimen of a toxic species should be considered equally poisonous. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing. Thus, the only way to avoid poisoning is to avoid consumption of the toxic species.

Poisonings in the United States occur most commonly when hunters of wild mushrooms (especially novices) misidentify and consume a toxic species, when recent immigrants collect and consume a poisonous American species that closely resembles an edible wild mushroom from their native land, or when mushrooms that contain psychoactive compounds are intentionally consumed by persons who desire these effects. Nature of Disease Mushroom poisonings are generally acute and are manifested by a variety of symptoms and prognoses, depending on the amount and species consumed. Because the chemistry of many of the mushroom toxins (especially the less deadly ones) is still unknown and positive identification of the mushrooms is often difficult or impossible, mushroom poisonings are generally categorized by their physiological effects. There are four categories of mushroom toxins: protoplasmic poisons (poisons that result in generalized destruction of cells, followed by organ failure); neurotoxins (compounds that cause neurological symptoms such as profuse sweating, coma, convulsions, hallucinations, excitement, depression, spastic colon); gastrointestinal irritants (compounds that produce rapid, transient nausea, vomiting, abdominal cramping, and diarrhea); and disulfiram-like toxins.

Mushrooms in this last category are generally nontoxic and produce no symptoms unless alcohol is consumed within 72 hours after eating them, in which case a short-lived acute toxic syndrome is produced. Diagnosis of Human Illness A clinical testing procedure is currently available only for the most serious types of mushroom toxins, the amanitins. The commercially available method uses a 3H-radioimmunoassay (RIA) test kit and can detect sub-nanogram levels of toxin in urine and plasma. Unfortunately, it requires a 2-hour incubation period, and this is an excruciating delay in a type of poisoning which the clinician generally does not see until a day or two has passed. A 125I-based kit which overcomes this problem has recently been reported, but has not yet reached the clinic. A sensitive and rapid HPLC technique has been reported in the literature even more recently, but it has not yet seen clinical application. Since most clinical laboratories in this country do not use even the older RIA technique, diagnosis is based entirely on symptomology and recent dietary history.

Despite the fact that cases of mushroom poisoning may be broken down into a relatively small number of categories based on symptomatology, positive botanical identification of the mushroom species consumed remains the only means of unequivocally determining the particular type of intoxication involved, and it is still vitally important to obtain such accurate identification as quickly as possible. Cases involving ingestion of more than one toxic species in which one set of symptoms masks or mimics another set are among many reasons for needing this information. Unfortunately, a number of factors (not discussed here) often make identification of the causative mushroom impossible. In such cases, diagnosis must be based on symptoms alone. In order to rule out other types of food poisoning and to conclude that the mushrooms eaten were the cause of the poisoning, it must be established that everyone who ate the suspect mushrooms became ill and that no one who did not eat the mushrooms became ill. Wild mushrooms eaten raw, cooked, or processed should always be regarded as prime suspects. After ruling out other sources of food poisoning and positively implicating mushrooms as the cause of the illness, diagnosis may proceed in two steps. The first step, outlined in Table 1 , provides an early indication of the seriousness of the disease and its prognosis.

As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged.

Associated Foods Mushroom poisonings are almost always caused by ingestion of wild mushrooms that have been collected by nonspecialists (although specialists have also been poisoned). Most cases occur when toxic species are confused with edible species, and a useful question to ask of the victims or their mushroom-picking benefactors is the identity of the mushroom they thought they were picking. In the absence of a well- preserved specimen, the answer to this question could narrow the possible suspects considerably. Intoxication has also occurred when reliance was placed on some folk method of distinguishing poisonous and safe species. Outbreaks have occurred after ingestion of fresh, raw mushrooms, stir-fried mushrooms, home-canned mushrooms, mushrooms cooked in tomato sauce (which rendered the sauce itself toxic, even when no mushrooms were consumed), and mushrooms that were blanched and frozen at home. Cases of poisoning by home-canned and frozen mushrooms are especially insidious because a single outbreak may easily become a multiple outbreak when the preserved toadstools are carried to another location and consumed at another time. Specific cases of mistaken mushroom identity appears frequently.

The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra . Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta . The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3 . Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus , Lactarius, Russula , Tricholoma, Coprinus , Pluteus, and others. The Inky Cap Mushroom ( Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned.

Some other members of the genus Coprinus (Shaggy Mane, C. comatus ; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided. Most of the psychotropic mushrooms ( Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom ( Psilocybe cubensis ) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible.

Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom ( Marasmius oreades ) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom ( Gymnopilus spectabilis ), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap ( Amanita pantherina ) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A.

pantherina varieties are the Yellow Blusher ( Amanita flavorubens ). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom ( Armillariella mellea ). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs. Relative Frequency of Disease Accurate figures on the relative frequency of mushroom poisonings are difficult to obtain. For the 5-year period between 1976 and 1981, 16 outbreaks involving 44 cases were reported to the Centers for Disease Control in Atlanta (Rattanvilay et al. MMWR 31(21): 287-288, 1982). The number of unreported cases is, of course, unknown. Cases are sporadic and large outbreaks are rare. Poisonings tend to be grouped in the spring and fall when most mushroom species are at the height of their fruiting stage.

While the actual incidence appears to be very low, the potential exists for grave problems. Poisonous mushrooms are not limited in distribution as are other poisonous organisms (such as dinoflagellates). Intoxications may occur at any time and place, with dangerous species occurring in habitats ranging from urban lawns to deep woods. As Americans become more adventurous in their mushroom collection and consumption, poisonings are likely to increase. Course of Disease and Complications The normal course of the disease varies with the dose and the mushroom species eaten. Each poisonous species contains one or more toxic compounds which are unique to few other species. Therefore, cases of mushroom poisonings generally do not resembles each other unless they are caused by the same or very closely related mushroom species. Almost all mushroom poisonings may be grouped in one of the categories outlined above. PROTOPLASMIC POISON Amatoxins Several mushroom species, including the Death Cap or Destroying Angel ( Amanita phalloides , A. virosa), the Fool's Mushroom ( A. verna ) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins.

Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver.

Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney. Target Populations All humans are susceptible to mushroom toxins. The poisonous species are ubiquitous, and geographical restrictions on types of poisoning that may occur in one location do not exist (except for some of the hallucinogenic LBMs, which occur primarily in the American southwest and southeast). Individual specimens of poisonous mushrooms are also characterized by individual variations in toxin content based on genetics, geographic location, and growing conditions. Intoxications may thus be more or less serious, depending not on the number of mushrooms consumed, but on the dose of toxin delivered. In addition, although most cases of poisoning by higher plants occur in children, toxic mushrooms are consumed most often by adults. Occasional accidental mushroom poisonings of children and pets have been reported, but adults are more likely to actively search for and consume wild mushrooms for culinary purposes. Children are more seriously affected by the normally nonlethal toxins than are adults and are more likely to suffer very serious consequences from ingestion of relatively smaller doses. Adults who consume mushrooms are also more likely to recall what was eaten and when, and are able to describe their symptoms more accurately than are children.

Very old, very young, and debilitated persons of both sexes are more likely to become seriously ill from all types of mushroom poisoning, even those types which are generally considered to be mild. Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected. Food Analysis The mushroom toxins can with difficulty be recovered from poisonous fungi, cooking water, stomach contents, serum, and urine. Procedures for extraction and quantitation are generally elaborate and time-consuming, and the patient will in most cases have recovered by the time an analysis is made on the basis of toxin chemistry. The exact chemical natures of most of the toxins that produce milder symptoms are unknown.

Chromatographic techniques (TLC, GLC, HPLC) exist for the amanitins, orellanine, muscimol/ibotenic acid, psilocybin, muscarine, and the gyromitrins. The amanitins may also be determined by commercially available 3H-RIA kits. The most reliable means of diagnosing a mushroom poisoning remains botanical identification of the fungus that was eaten. An accurate pre-ingestion determination of species will also prevent accidental poisoning in 100% of cases. Accurate post-ingestion analyses for specific toxins when no botanical identification is possible may be essential only in cases of suspected poisoning by the deadly Amanitas, since prompt and aggressive therapy (including lavage, activated charcoal, and plasmapheresis) can greatly reduce the mortality rate. Selected Outbreaks Isolated cases of mushroom poisoning have occurred throughout the continental United States. The popular interest in gathering and eating uncultivated mushrooms has been associated with an increase in incidents of serious mushroom-related poisonings.

From December 28, 1996, through January 6, 1997, nine persons in northern California required hospitalization after eating Amanita phalloides (i.e., "death cap") mushrooms; two of these persons died. Risks associated with eating these mushrooms result from a potent hepatotoxin. This report describes four cases of A. phalloides poisoning in patients admitted to a regional referral hospital in northern California during January 1997 and underscores that wild mushrooms should not be eaten unless identified as nonpoisonous by a mushroom expert. Another one occurred in Oregon in October,1988, and involved the intoxication of five people who consumed stir-fried Amanita phalloides . The poisonings were severe, and at this writing three of the five people had undergone liver transplants for treatment of amanitin-induced liver failure.

Other cases have included the July, 1986, poisoning of a family in Philadelphia, by Chlorophyllum molybdites ; the September, 1987, intoxication of seven men in Bucks County, PA, by spaghetti sauce which contained Jack O'Lantern mushroom (Omphalotus illudens); and of 14 teenage campers in Maryland by the same species (July, 1987). A report of a North Carolina outbreak of poisoning by False Morel ( Gyromitra spp.) appeared in 1986. A 1985 report details a case of Chlorophyllum molybdites which occurred in Arkansas; a fatal poisoning case caused by an amanitin containing Lepiota was described in 1986. In 1981, two Berks County, PA, people were poisoned (one fatally) after ingesting Amanita phalloides , while in the same year, seven Laotian refugees living in California were poisoned by Russula spp.

In separate 1981 incidents, several people from New York State were poisoned by Omphalotus illudens , Amanita muscaria, Entoloma lividum , and Amanita virosa. An outbreak of gastroenterititis during a banquet for 482 people in Vancouver, British Columbia, was reported by the Vancouver Health Department in June, 1991. Seventy-seven of the guests reported symptoms consisting of early onset nausea (15-30 min), diarrhea (20 min-13 h), vomiting (20-60 min), cramps and bloated feeling. Other symptoms included feeling warm, clamminess, numbness of the tongue and extreme thirst along with two cases of hive-like rash with onset of 3-7 days. Bacteriological tests were negative. This intoxication merits special attention because it involved consumption of species normally considered not only edible but choice. The fungi involved were the morels Morchella esculenta and M. elata ( M. angusticeps ), which were prepared in a marinade and consumed raw. The symptoms were severe but not life threatening. Scattered reports of intoxications by these species and M.

conica have appeared in anecodotal reports for many years. Numerous other cases exist; however, the cases that appear in the literature tend to be the serious poisonings such as those causing more severe gastrointestinal symptoms, psychotropic reactions, and severe organ damage (deadly Amanita ). Mild intoxications are probably grossly underreported, because of the lack of severity of symptoms and the unlikeliness of a hospital admission. US Food and Drug Administration Trusted Amanitaceae: Amanita fungi picture gallery Taxonomic history of the genus Amanita Amanita phalloides (Deathcap) The Amanita genus, which contains more than 600 species worldwide, was first named (with its present meaning and with the Fly Agaric, Amanita muscaria , as the 'type species') in 1797 by Christiaan Hendrik Persoon . Etymology The origin of the genus name Amanita is lost in the mists of time. Several alternative hypotheses have been out forward, but one that many authorities suggest is credible is that it is in some way a reference to Mount Amanon, a mountain in Cicilia overlooking the north-eastern Mediterranean.

This group of agarics (fungi with caps and gills mounted upon a stem) is well know for the prized edible Caesar's Mushroom ( Amanita caesarea ) as well as several deadly poisonous species - Amanita phalloides and Amanita virosa , for example. This group also contains Amanita muscaria , commonly known as the Fly Agaric, one of the most beautiful of all the gilled fungi. The Death Cap and Other Poisonous Amanita Mushrooms > The Death Cap and Other Amanita Mushrooms The Deadly Death Cap and Other Amanita Mushrooms With names referencing death and destruction, it's no wonder the Amanita mushroom genus contains some of the most famous and deadly of all poisonous mushrooms. The death cap (Amanita phalloides) is suspected to have caused more mushroom poisoning deaths than any other species! Yet what makes some amanita mushrooms so poisonous? Certain species of Amanita contain amanitin, a deadly amatoxin. Amatoxins are some of the most lethal poisons found in nature. These toxins work by slowly shutting down the liver and kidneys. Often the victim will appear sick at first, and then seem to get better.

Unfortunately the amatoxins are still at work, and death may occur anywhere from a few days to a week after ingestion. This poison knows no real antidote beyond treating the victim with an extract of milk thistle. Milk thistle protects against liver damage from toxins, and is one of the treatments for amanita mushroom poisoning. Despite this treatment, it's said that one cap of a death cap is enough to kill. Given the danger, we'd better learn some poisonous mushroom identification! Visit this page to learn how to identify poisonous amanita mushrooms in general. Remember: Never solely identify any mushroom based on what you've seen on any website (including this one) or by comparing it to a picture in a book. Always obtain hands-on expert help when identifying a new mushroom and never eat anything you're not sure of! Between 3 to 6 inches across Convex initially but flattens with age, often sticky when touched Color is usually a shade of yellow to green, but sometimes white or brownish White gills underneath the cap that don't run down the stem Stem Between 3 to 6 inches across and less than an inch thick Usually whitish, sometimes with scales Often a ring around the stem right below the cap.

This ring is the remnant of the partial veil, a piece of tissue that protected the mushroom's gills as it grew. Also present is a white sac around the base of the stem. All amanita mushrooms start their lives as small buttons in the shape of an egg. This egg-like covering is actually a layer of tissue called the universal veil, or volva. Because they form as a small button, an amanita may sometimes be mistaken for an edible puffball. This is why it's essential to slice a puffball open before eating it. Puffballs are white and solid on the inside with no gills. If you see gills, you may have an amanita on your hands. Once the mushroom has grown, the sac-like remnants of this universal veil are still an important identification characteristic. It's often underground so you may have to dig carefully around the base to find it. However, never assume that you don't have an amanita mushroom just because you can't find the sac. It may have disintegrated or broken away. Use all features for poisonous mushroom identification, not just one! Spore print White Habitat The death cap, like all Amanita species, is suspected to be mycorrhizal.

This means the mycelium of the mushroom forms a symbiotic relationship with the roots of trees. For this reason they are found on the ground in the woods, although occasionally they will occur in grassy fields. Often found near oak and pine trees. Sometimes seen near other hardwoods such as chestnut, beech, birch, and spruce. Time of year Late August through November, or whatever passes as late-summer to late fall in your area. Distribution The death cap is originally a European mushroom, and is found throughout Europe and parts of North Africa. The species was introduced to North America and is most often seen in California. However, there are reports of it in many other states including Pennsylvania, Ohio, and parts of the East Coast. Click here for a great article about a biologist studying the this mushroom in California. Shipping wood, lumber, and live seedlings has introduced the species to other parts of the world, such as Australia and parts of South America. Assume the death cap, or some other poisonous mushroom, lives where you live! Other Infamous Amanitas No page on poisonous mushrooms would be complete without discussing the death cap's deadly cousin, the destroying angel.

The term "destroying angel" actually refers to a few all-white poisonous mushrooms in the Amanita genus. They are: Amanita bisporigera in Eastern North America Amanita ocreata in Western North America Amanita virosa in Europe (below) Amanita virosa is known as the "European destroying angel". There is some disagreement as to whether this mushroom exists in the United States. Destroying angels are sometimes mistaken for edible mushrooms such as young puffballs, button mushrooms, and meadow mushrooms. Thus it's important to learn how to identify them. The destroying angel is very similar to the death cap in terms of identification. The biggest difference is that they're all white, with no green or yellow tint. They're recognized by their rounded base, white color, and smooth cap. One bite of these may contain enough amatoxins to kill! Of course, not every species in the Amanita mushroom genus is poisonous. Some, such as Amanita caesarea (Caesar's mushroom) , are edible. Yet given the danger involved in eating the wrong amanita, it's best to avoid the genus entirely unless you really know what you're doing.

It's important to learn how to recognize Amanitas (especially the death cap and the destroying angel) if one is going to start eating wild mushrooms. Proper knowledge can prevent a fatal mistake! Be safe! Return to top The first picture was taken by Archenzo and is published on Wikipedia under the GNU Free Documentation License. The last picture was taken by Eric Steinert and is published on Wikipedia under the GNU Free Documentation License. Amanita Poisoning Amanita phalloides Introduction NO MUSHROOM is worthier of fear than the terribly poisonous Death Cap (Amanita phalloides). This single, widespread species of mushroom is solely responsible for the majority of fatal and otherwise serious mushroom poisoning cases, worldwide as well as in North America. Indeed, one might argue that the Death Cap's notorious, relatively frequent victimization of Homo sapiens is far and away the best explanation (or rationalization) for the widespread fear of edible wild mushrooms. This is the EXACT reason that the infamous Amanita muscaria mushroom, which is an edible mushroom in countless cultures, has been labeled as a poison by the FDA. It was in the same family as the deadliest mushroom known to man, but it is not the poisonous variety.

If there was a berry this bad... Ecology and Range of A. phalloides in North America This mushroom is rare in most parts of North America but locally common in such areas as the San Francisco Bay area, where it is typically found from mid-autumn through late winter. Primarily a European species, there is no evidence that the Death Cap is native to North America. Ecologically, it is a beneficial mycorrhizal fungus---it lives on the roots of live trees, providing phosphorus, magnesium, and other nutrients to the tree in exchange for carbohydrates. In California, it occurs under live oak and cork trees (it apparently was brought in with cork tree seedlings, and has since adapted to native oaks). There is a similar situation in the Irondequoit area north of Rochester, New York: the Death Cap was first discovered in Durand-Eastman Park in the 1970s under Norway spruce trees that had been imported as nursery stock decades earlier. It has since been found in increasing numbers and in an ever-enlarging but still local range, under native oaks; it is rather reliably found there from late September through late October. The Death Cap has also been reported under oaks in southern Oregon.

"The Southeast Asian Problem" There are other mushrooms which are as poisonous---or nearly as poisonous---as A. phalloides, but this one species causes far more poisonings than the others. There is an explanation for this. Most victims of life-threatening mushroom poisoning in North America are people from Southeast Asia---Laos, Cambodia, Thailand, Viet Nam. They apparently mistake Death Caps for edible "Paddy-Straw" (Volvariella volvacea) mushrooms. The two are similar in several ways---cap color, size, and the white "cup" around the base of the stalk---but different in others (for example, the Paddy-Straw has a pink spore print, the Death Cap a white spore print; and the Death Cap has a partial veil). The Paddy Straw mushroom occurs in tropical and temperate areas worldwide, and is especially common in Southeast Asia; the Death Cap, alas, does not occur in Southeast Asia, so folks from that part of the world are unaware of the lethal "look-alike." Consider the following---a revealing comment from USENET: bionet.mycology (June 1997): "My wife comes from Thailand.

Last Fall, we were strolling through our woods when she spied a mushroom. She was overjoyed to find that America, too, has straw mushrooms, and assured me it was edible. Knowing even less about mushrooms than I do now, but knowing the danger of not knowing, I advised her to leave it alone. ...the specimen did indeed resemble a straw mushroom, except for the presence of a ring on the stipe [stalk]." --Tim Childress In North America, Death Cap poisonings have been reported from California, Oregon, and New York. In New York, the only known victims to date were natives of Laos. In California and in Oregon, most reported Death Cap poisonings have also involved Southeast Asian immigrants. The poisoning cases typically involve several victims---often including children---who "enjoyed" the mushrooms as a group. One or two deaths per case are common. The treatment of choice is often liver transplantation. Especially with early diagnosis, other effective treatments include massive doses of penicillin, which stimulates the liver's defenses. The Death Cap should be sought in every part of North America where Norway spruce or cork trees have been cultivated.

If found, its presence should be publicized locally, regionally, and nationally to reduce the risk of further tragedies. It is especially vital to educate communities of Southeast Asian immigrants about this lethal mushroom. Causes of Serious Mushroom Poisonings The "but I thought it was edible..." phenomenon, where the victims either thought they "knew" the mushroom species or applied some folk myth such as "no poisonous mushrooms grow on wood," is one of four causes of mushroom poisoning in humans. Another often-tragic cause is similar---an individual eating a dangerously toxic wild mushroom in the belief (or with the hope) that it is a hallucinogenic species. The most common cause of mushroom exposures, by far, is infant and toddler "grazing"---where young children ingest mushrooms as a way of experiencing their environment. (This phenomenon is also commom with domestic dogs!) Sadly, in many areas, physicians automatically opt for traumatic treatment via Epicac, even in cases in which the patient shows no symptoms and uneaten specimens are available for examination, without consulting a mycologist to attempt to determine the identity and toxicity of the mushroom.

Incredibly enough, the fourth cause of mushroom poisoning is simple foolishness: a false presumption that most mushrooms are safe, and/or that poisonous mushrooms "look," "taste," or "smell" bad. (As many victims of Death Cap poisoning can attest, that is not true!) The Death Cap (Amanita phalloides): A Simple Mushroom to Identify The Death Cap can be easily diagnosed as such. The cap is 2ï¿½--6" (6--16 cm) wide, smooth, with greenish to yellowish pigments, usually sticky or slippery but sometimes dry, often adorned with one to several patches of thin white veil tissue. The gills are white, crowded together, and very finely attached to the upper stalk. In young specimens, a white, membranous partial veil tissue extends from the edge of the cap to the upper stalk, covering the gills (later remaining attached to and draping from the upper stalk). The stalk is white to pallid, up to 6" (15 cm) long or tall, with a large rounded bulb at the base; the bulb includes a white sac-like volva (see the two photos on this webpage).

THE BASE OF THE STALK AND THE TELL-TALE VOLVA ARE OFTEN BURIED IN THE SOIL. Equally Toxic North American Mushrooms Amatoxins contained in the Death Cap are responsible for the symptoms suffered by its victims. They are present in all the tissues of the mushroom, in sufficient concentration that two or three grams are considered a potentially lethal dose. Several other species in genus Amanita---most notably the all-white "Destroying Angels" (A. virosa, A. bisporigera, and A. verna)---contain comparable levels of amatoxins. Moreover, several species of other genera of gilled mushrooms (notably Conocybe filaris, Galerina autumnalis and G. venenata, and Lepiota josserandii and L. helveola) also contain these toxins. Conocybe filaris is a dainty, fragile species unlikely to be considered as food, but it may pose a "grazing" danger to small children and to dogs.

Galerina venenata is a small, uncommon brown mushroom sometimes found on lawns in the Pacific Northwest; it is unlikely to be considered as potential food, but it poses a "grazing" danger to small children and to dogs. Galerina autumnalis is a small brown mushroom that grows on dead/decaying wood; mushroom enthusiasts must be diligent to avoid inadvertently picking specimens of this species while harvesting more robust edbile mushrooms that grow on wood. Genus Lepiota includes several worthwhile edible species of much larger stature than the diminutive species shown to contain amatoxins; mushroom enthusiasts must be diligent to avoid small Lepiotas, as at least one fatality has resulted from this genus in North America.

(Note: a close relative of the Lepiotas---Chlorophyllum molybdites, the "Green-spored Lepiota"---contains unrelated toxins that cause severe gastrointestinal symptoms; while ingestion of this species is not generally life-threatening, it can cause dehydration severe enough to require hospitalization for fluid and electrolyte maintenance.) The Destroying Angels ---Amanita virosa and other closely related white Amanitas---have been consumed by ignorant collectors, both as food and, in at least one case, under the mistaken notion that they might be hallucinogenic. Visually, the Destroying Angel is very similar to its more notorious brother; the most notable difference is the lack of green or yellow pigments (though some slight yellowing may be observed on some specimens). Like the Death Cap, the Destroying Angel is a very easily identified mushroom. The cap of the Destroying Angel is 2ï¿½--6" (6--16 cm) wide, smooth, dry to slightly sticky. The gills are crowded together and may appear either very finely attached to the upper stalk or unattached.

In young specimens, a white, membranous partial veil tissue extends from the edge of the cap to the upper stalk, covering the gills (later remaining attached to and draping from the upper stalk, but it is very thin and fragile, hence is sometimes not seen on mature specimens). The stalk is white to pallid, up to 8" (21 cm) long or tall, with a small, rounded bulb at the base; the bulb is enclosed by a sac-like volva. All parts of the Destroying Angel are white. THE BASE OF THE STALK AND THE TELL-TALE VOLVA ARE OFTEN BURIED IN THE SOIL. The Destroying Angels are common and widespread throughout much of North America; the danger of these easily-identified species---and their identifying traits---ought to be widely taught in elementary school and beyond. -- Edible Wild Mushrooms of North America by Fischer and Bessette (1992, Univ.

of Texas Press, Austin) The delay before onset of symptoms, coupled with the intitial symptoms' mimicry of influenza and other gastrointestinal viruses and the marked (albeit temporary) improvement of most patients beginning two or three days after ingestion, pose inherent problems in prompt diagnosis and treatment. In cases where early diagnosis is accomplished, effective therapies have included massive doses of penicillin and other compounds which pharmacologically inhibit the amatoxins from effecting their most severe liver damage. In more severe cases, especially those in which diagnosis is delayed further by failure to suspect amatoxin poisoning, liver transplant is the preferred therapy. For most patients, full recovery to their states of health prior to hospitalization is unlikely. "The Sky is Falling!" Death Cap Poisonings Elicit Overreactive Statements In California, in January, 1997, some folks picked some wild mushrooms, cooked and ate them, without knowing what they were doing... without consulting a good mushroom field guide... without carefully comparing specimens to descriptions and photos... in short, without properly identifying the mushrooms they picked. Once again, the mushrooms they picked were "Death Caps" (Amanita phalloides). Once again, folks ended up with serious liver damage; several of them died.

And, once again, some authorities spouted overreactive nonsense, not merely implying but explicitly stating that it is inherently dangerous for anyone but an "expert" to pick and eat wild mushrooms. The Associated Press reported (1/8/97): An outbreak of wild mushroom poisonings has sickened at least nine people in Northern California, with three victims in intensive care Wednesday facing possible liver transplants. The most seriously ill were felled by the "death cap'' mushroom, known technically as Amanita phalloides, which can destroy the liver. One victim was Sam Sebastiani Jr., 31, a member of the Sebastiani wine family. The Mushroom Council, which represents commercial mushroom producers and importers throughout the United States, said this in a news release: The Mushroom Council urges the public to be extremely cautious when foraging for wild mushrooms outside, especially in fields and forests, because of potential health dangers that can be caused by some wild varieties [sic]... The untrained and uneducated person can make an innocent mistake when hunting wild mushrooms that could result in illness or even death... Commercially produced mushrooms that are in your supermarket or in prepared foods are carefully cultivated agricultural products, grown year around.

This was, perhaps, neither terribly unreasonable, nor terribly overreactive. It certainly was opportunistic for the Mushroom Council to steer consumers toward their industry's produce---and away from the free foods of the forests and fields---in the capitalist tradition. No one can blame them for that. Indeed, it can be argued that some folks would hear the news stories and react with a fear of all mushrooms, including the safe cultivated species, so the Mushroom Council was merely trying to mitigate against the danger of public misperception. Editorial note: Never mind that some of the most widespread cases of serious poisoning by mushrooms in North America has been the result of botulism caused by errors in the canning of commercially cultivated mushrooms... and be sure to take a good look at those "fresh" mushrooms in the produce department of your favorite grocery store, for this "short-shelflife" commodity often shows serious signs of decay at the supermarket. The problem here is that "untrained and uneducated" can be misinterpreted as "lacking formal training and education in mycology"... and that is simply not true.

Rose Ann Soloway, administrator of the American Association of Poison Control Centers, had this to say (and The Mushroom Council plugged it into their news release): It is our strong recommendation that people not pick and eat wild mushrooms unless they, in fact, are experts, or the person identifying the mushrooms is someone with whom they would trust their life. Hmmm... "expert"? What, exactly, is an expert? Better question: how much of an "expert" should one be to identify wild mushrooms for human consumption? The Truth Millions of North Americans pick and eat wild mushrooms every year, without as much as a belly ache. Are they "experts"? Yes! At least, they are experts on the edible wild mushrooms they know. Either their parents or grandparents taught them how to identify morels, or puffballs, or meadow mushrooms, or they have a good field guide and they read it... or both. No one with a reasonable understanding of the importance of properly identifying mushrooms---with a serious awareness that some species are fatally toxic---falls victim to the Death Cap. The folks who eat Death Caps do not use field guides: they just pick the damned things and eat them. No trip to the library. No reading. No spore prints.

No idea what a "partial veil" is or what "gill attachment" means. So... Is it really dangerous to eat wild mushrooms? How dangerous is it to drive a car? If you're drunk or careless, it is VERY dangerous; if you're sensible and pay attention, it is reasonably safe. Consider this: Would you pick and eat an unfamiliar berry simply because it "looked good"? Of course not. Finding, identifying, preparing, and eating wild mushrooms can be a delightful pasttime---IF it is done intelligently. Otherwise, it is a terrible "accident" waiting to happen. Copyright ï¿½1997 by David W. Fischer. All rights reserved. This site maintained by David W. Fischer, whose e-mail address is [email protected] .

Question: The poisonous fungus Amanita Phalloides is better known by what name?
Answer: The Death Cap